The Head-Shaking Test In The Horizontal Plane

In this interview, Dr. Vincenzo Marcelli delves into the head-shaking test (HST) in the horizontal plane, a diagnostic tool used in the clinical evaluation of vestibulopathic patients. Dr. Marcelli elaborates on the purpose, execution, and clinical interpretation of the test, both for peripheral and central vestibular lesions, and discusses the instrumental advancements that enhance the diagnostic process, including Nystalyze, a modular, state-of-the-art VNG system by Inventis.

 

AudiologyOnline: Could you tell us about the historical background and purpose of the head-shaking test (HST) in clinical practice?

Dr. Vincenzo Marcelli: The concept that rapid head movement could generate nystagmus dates back to Bárány in 1907, but it was Vogel who introduced the head-shaking nystagmus (HSN) into clinical practice over 20 years later. The head-shaking test (HST) is one of the high-frequency tests used for the non-instrumental clinical evaluation of patients with vestibulopathies. The main purpose of this test is to evaluate the asymmetry of the dynamic gain of the vestibulo-ocular reflex (dg-VOR), which is generated by the lateral semicircular canal (CSL) or by dysfunctions in the central vestibular pathways.

AudiologyOnline: What frequency is typically explored during the HST, and what equipment is necessary for the test?

Dr. Vincenzo Marcelli: The test is conducted at a high frequency, around 2 Hz. Traditionally, Frenzel glasses or systems designed to eliminate visual fixation are used. However, it is worth noting that in some cases, the intensity of the nystagmus is so pronounced that it can be observed without specialized instruments, visible to the naked eye.

AudiologyOnline: Could you describe the procedure of the head-shaking test?

Dr. Vincenzo Marcelli: The test is typically executed following the guidelines established by Kamei (1). The patient is seated and wears Frenzel glasses (or another instrument that prevents visual fixation). The operator holds the patient’s head, which is inclined forward at about a 30-degree angle, and moves it side-to-side at a rate of approximately two movements per second (2 Hz), with a lateral excursion of about 45 degrees to each side, for a duration of around 15 seconds. After the shaking, the operator observes for any nystagmic response.

AudiologyOnline: What are the main mechanisms involved and how do they relate to the clinical findings of the HST?

Dr. Vincenzo Marcelli: To understand the method of execution and correctly interpret the findings it is necessary to remember that the HST is based on the integrated action between Ewald's second law, velocity storage mechanism (VSM) and the nodulus-uvula complex of the cerebellum (cNU).

1. Ewald's second law establishes a directional asymmetry according to which, for the same stimulus, excitation determines a more intense response than inhibition and this is due to the impossibility for an inhibitory stimulus to reduce the discharge frequency of the vestibular nerve below the zero (2).
2. The VSM stores and prolongs the vestibular signal over time, increases the time constant by approximately three times and improves vestibular performance at low stimulation frequencies (3).
3. Finally, cNU exerts inhibitory control over the VSM and the spatial orientation of the angular vestibulo-ocular reflex, allowing the response to occur in the stimulus plane (4, 5).

AudiologyOnline: What are the parameters to consider when analyzing the nystagmus response generated by the HST?

Dr. Vincenzo Marcelli: The nystagmus response is considered significant when at least five nystagmus shocks are detected (6). There are both qualitative and quantitative parameters to consider:

1. Qualitative parameters include the morphology (whether the response is monophasic or biphasic), the direction, the plane, and the intensity of the nystagmus.
2. Quantitative parameters are primarily focused on the duration of the response.

The possible responses will now be examined in case of asymmetry of the dynamic gain of the VOR due to peripheral pathology and in case of lesion affecting the central vestibular apparatus (AVC).

AudiologyOnline: What are the clinical interpretations of HST results in peripheral vestibular lesions?

Dr. Vincenzo Marcelli: In case of symmetry of the dg-VOR, the signals generated in the two CSLs during the HS will be of the same entity but of opposite sign, so the VSM cannot be loaded and no HSN will be generated.

On the contrary, in case of asymmetry, the asymmetric canal signals due to the prevalence of one hemisystem will generate a "positive energy balance" which will charge the VSM, which in turn is responsible for the HSN when stimulation stops.

We examine two possibilities: absence or presence of spontaneous nystagmus.

1. In the absence of spontaneous nystagmus, it will be possible to observe a horizontal-torsional nystagmus with a rapid phase directed towards the prevailing hemisystem, a typical finding for example of a vestibulopathy not yet compensated at high frequency: the so-called “paretic” HSN. However, the possibility cannot be excluded that HSN is directed toward the side known to be hypoactive in a kind of vestibular recruitment: as in the case of cochlear recruitment, when the stimulus is particularly intense (as in the case of head-shaking) the partially injured receptor may be activated more than the healthy receptor. Such a finding is discreetly frequent in Meniere's disease, for example.
2. In the presence of spontaneous nystagmus, it may be possible to observe:
   1. an increase in the frequency of the amplitude of the nystagmus, which supports the presence of a dynamic asymmetry of the VOR, the static one being already attested by the presence of spontaneous nystagmus.
   2. the lack of modification of spontaneous nystagmus. Two explanations are possible:
      1. in the acute phase of a peripheral vestibulopathy or in the case of a complete unilateral deficit, the VSM could be deactivated “to protect” the patient (7) since a long duration of the constant VOR time would greatly accentuate the symptoms with even the slightest movement of the head; deactivating the VSM will therefore not allow any HSN to be generated;
      2. b. the nystagmus does not change because it is determined by a lesion to the AVC: in such cases a peripheral stimulus such as the HSN generally has no effect;
   3. the reversal of the direction of spontaneous nystagmus. At least three explanations are possible:
      1. the nystagmus is of “recovery” type and is directed towards the hypoactive side, while the HSN is directed towards the healthy side; the “recovery” nystagmus can be the expression of:
         1. an imbalance of vestibular nuclei with prevalence of the previously hypoactive hemisystem, which is now the site of static reorganization,
         2. the expression of the recovery of the receptor function;
      2. spontaneous nystagmus is of “irritative” type and is directed towards the hypoactive side while the HSN is directed towards the healthy side; this finding is frequent for example in the case of Menière disease where it is possible to observe a spontaneous nystagmus directed towards the affected side, an ipsilateral deficit confirmed by V-HIT and an HSN directed towards the healthy side (personal observation); this “irritative” nystagmus is generated by a mechanic distortion of the cupula due to a translabyrinthine dilational pressure P0 in response to hydrops.
      3. spontaneous nystagmus beats towards the prevailing side while HSN directed contralaterally toward the hypoactive labyrinth is the result of a labyrinthine recruitment which, like cochlear recruitment, is generated with particularly intense stimuli such as head-shaking and vibration. In this regard, it is important to clarify a concept: although reported in the literature, we tend to exclude that, in such cases, the HSN is of “recovery” type: in fact, it is difficult to understand how a hypoactive hemisystem from a static point of view can instead be prevalent, compared to the contralateral one, from a dynamic point of view.

In each of the possible cases reported, the response may be monophasic or biphasic.

The monophasic response is characterized by the presence of nystagmus that always beats in the same direction for the entire observation time. As already mentioned, the HSN is defined as “paretic” if it is directed towards the side that is prevalent at that specific moment in the patient's clinical history; on the contrary, it is defined as “recovery” if it is directed towards the side considered hypoactive. In our experience, this finding is not frequently encountered; it may in fact be present in a rather narrow time window during the dynamic and high-frequency recovery phase of the previously affected hemisystem which becomes temporarily dominant compared to the healthy hemisystem, still inhibited by the cerebellar structures to reduce the static-dynamic asymmetry.

The biphasic response is characterized by a nystagmus which, after an initial intense phase directed towards one side, spontaneously reverses its direction, giving rise to the second phase. The explanation would be to be found in the fact that the first phase, especially if particularly intense, would determine a functional exhaustion of the peripheral but more likely central vestibular structures and a consequent transitory prevalence of the contralateral structures. In any case, the second phase is not related to the recovery of the peripheral receptor.

AudiologyOnline: What about HST results in central vestibular lesions?

Dr. Vincenzo Marcelli: In clinical practice, the two central HSN patterns are represented by the perverted HSN (p-HSN) and the minimal stimulus HSN (ms-HSN).

By p-HSN after HS on the horizontal plane we mean the appearance of a nystagmus on the sagittal plane (down beat or up beat nystagmus) or frontal plane (clockwise or anticlockwise torsional) which clearly prevails over any concomitant horizontal nystagmus, or the variation of the plane of a horizontal spontaneous nystagmus. The lesion in this case is to be found in a cNU suffering, with loss of spatial orientation of the angular vestibulo-ocular reflex and inability to match the response plane with the stimulus plane.

By sm-HSN we mean the appearance of a nystagmus after very few cycles of head rotations (even 2-3) performed at a very low speed, a stimulus not capable of generating a “quantity” of energy sufficient to load the VSM. The ms-HSN thus evoked, regardless of the plane in which it strikes, is suggestive of a lesion of the cNU: the loss of the inhibitory control exercised by this complex on the VSM allows the latter to load and generate even particularly long nystagmic responses with minimal stimuli. Therefore, in the presence of a very strong HSN generated with stimulation of 15 seconds, it is always very important to perform a HS with minimal stimulation.

AudiologyOnline: How does modern instrumentation, such as Nystalyze by Inventis, impact the execution and analysis of the HST?

Dr. Vincenzo Marcelli: The introduction of advanced systems like Nystalyze has revolutionized the way we approach vestibular diagnostics. Nystalyze is a modular, state-of-the-art VNG system that delivers an exceptional user experience with its three different modules and wireless camera. This technology not only improves the accuracy and precision of vestibular assessments, such as the head-shaking test, but also enhances patient comfort and the overall diagnostic process. The ability to record and analyze the nystagmus response in real time, with such a high level of detail, allows clinicians to make more informed decisions regarding treatment options for patients suffering from dizziness and vertigo.

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